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Frequent testicular involvement in multibacillary leprosy

Hendra Gunawan, Pati Aji Achdiat, Rachel Marsella Rahardjo, Reti

Hindritiani, Oki Suwarsa

PII: S1201-9712(19)30406-0
DOI: https://doi.org/10.1016/j.ijid.2019.10.013
Reference: IJID 3789

To appear in: International Journal of Infectious Diseases

Received Date: 5 August 2019

Revised Date: 7 October 2019
Accepted Date: 13 October 2019

Please cite this article as: Gunawan H, Achdiat PA, Rahardjo RM, Hindritiani R, Suwarsa O,
Frequent testicular involvement in multibacillary leprosy, International Journal of Infectious
Diseases (2019), doi: https://doi.org/10.1016/j.ijid.2019.10.013

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© 2019 Published by Elsevier.

ORIGINAL ARTICLE

Frequent testicular involvement in multibacillary leprosy

Hendra Gunawana,*, Pati Aji Achdiata, Rachel Marsella Rahardjoa, Reti Hindritiania, Oki

Suwarsaa
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Department of Dermatology and Venereology, Faculty of Medicine, Universitas Padjadjaran-

Dr. Hasan Sadikin Hospital, Bandung 40161, West Java, Indonesia

Short title Testicular involvement in leprosy

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Manuscript word: Body text 2462, Abstract count 199, Figure 1, Table 5

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Correspondence

Hendra Gunawan
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Department of Dermatology and Venereology
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Faculty of Medicine, Universitas Padjadjaran - Dr. Hasan Sadikin Hospital
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Bandung 4016 Indonesia

Phone: +62222032426 ext. 3449

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E-mail: endaguna@yahoo.com
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Highlights

 Testicular damage may occur before and while taking antileprotic treatment
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 Testicular involvement in leprosy might occur in the absence of signs and symptoms

 The assessment of testicular function should be recommended as a routine work-up for

leprosy patients

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Abstract

Objective Testicular involvement or atrophy is silent, unreported, and under-estimated in

leprosy. This study aims to assess the frequency of testicular atrophy and its consequences

through the examination of clinical manifestation, hormonal profile, and semen analysis in

leprosy patients.

Methods We conducted a descriptive observational study using a cross-sectional design and

consecutive sampling method from May to July 2018. This study was conducted in Dr. Hasan

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Sadikin General Hospital, Bandung, Indonesia and included 32 men affected by leprosy and

five healthy men as control group. All patients were subjected to history taking,

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dermatological and genital examination, assessment of follicular stimulating hormone (FSH),
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luteinizing hormone (LH), testosterone, and testicular ultrasonography examination. Semen

analysis was performed in 10 patients who consented.

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Results Testicular atrophy was observed in 93.75% patients. Clinical manifestations of
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testicular atrophy was loss of libido (21.87%), female pubic hair pattern (9.38%),

gynecomastia (6.25%), and secondary infertility (6.25%). Hormonal imbalance was seen in

16 patients and all ten patients undergone semen analysis showed abnormality.
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Conclusion This study showed a high frequency of testicular atrophy but the symptoms only

presence in a few of patients. The assessment of testicular function should be recommended

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as a routine work-up for leprosy patients.

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Keywords Leprosy, Male fertility, Testicular atrophy, Testosterone

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Introduction

Leprosy is a slowly-progressive and chronic systemic granulomatous disease caused by

Mycobacterium leprae (M. leprae), an obligatory intracellular organism (Hasan et al., 2017;

Leal and Foss, 2009). Leprosy primarily affects the skin and peripheral nerves and

secondarily involves internal organs like eyes, bones, lymph nodes, and the testicles (Hasan et

al., 2017; Saporta and Yuksel, 1994). An invasion of M. leprae to the testicles leads to

testicular atrophy and gonadal hormone imbalance (Achdiat et al., 2018). Testicular atrophy is

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defined as decrease of testicular size or volume because of testicular shrinkage following

invasion of M. leprae and subsequent inflammation in the testis with or without loss of

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function (Migam et al., 1984; El-Beheiry et al., 1979).
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There is great variability in the reported frequency of testicular involvement or atrophy in

leprosy, ranging from 10 to 50% (Saporta and Yuksel, 1994). In other study, about 50% of the
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screened lepromatous patients had hormonal changes suggestive of unsuspected testicular
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involvement. Testicular atrophy is often silent, unreported, and remain undiagnosed in

leprosy patients. These disorders usually asymptomatic and occur late in the course of the

disease (Singh et al., 2015). Although testicular involvement in leprosy has long been
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recognized, sexual disability and infertility has not received much attention (Leal and Foss,

2009; Singh et al., 2015).

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The testicles act as a reservoir for M. leprae and the bacilli reach the testicles via the
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lymphatic system, blood or by direct invasion through the adjacent skin tissue (Andrade et al.,

2012). The reason behind the testicles being the predilection site of the bacilli is not well

understood and it is accepted that the lower temperature in the testicles, compared to higher

internal body temperature, may facilitate the growth of M. leprae (Leal and Foss, 2009). The

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mechanism of testicular atrophy includes immune response alteration mediated by

inflammatory cytokines and local changes due to endarteritis and fibrosis (Singh et al., 2015).

Leprosy affects both seminiferous tubules and the Leydig cells, leading to an increase in

luteinizing hormone (LH) or follicle stimulating hormone (FSH) (Hasan et al., 2017;Andrade

et al., 2012). Testicular atrophy manifests as decrease testosterone production causing altered

sexual function. Defect in spermatogenesis may also lead to infertility (Hasan et al., 2017).

Several factors may contribute to testicular atrophy, including the degree of testicular

involvement, duration of disease, early treatment, and frequency of orchitis resulting from

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erythema nodosum leprosum (ENL) (Elkawi et al., 2014).

Comprehensive analysis of testicular atrophy in leprosy is not widely studied, and there is

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limited research on this subject in Indonesia. Therefore, we conducted this study to assess the
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frequency of testicular atrophy and its consequences through the examination of clinical

manifestation, hormonal profile, and semen analysis in men affected by leprosy.

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Methods

Study Subjects

a. Patients group
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This study included 32 men affected by leprosy, Sundanese, aged 15-40 years old,

obtained through consecutive sampling. They were either receiving multi-drug therapy
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(MDT) for leprosy or were released from treatment (RFT). Exclusion criteria were
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(1) patients with diabetes, tuberculosis, hepatic or renal affection, as were evaluated through

history taking and physical examination; (2) patients with history of chemotherapy or

radiotherapy; and (3) patients who had history of parotitis and testicular abnormalities due to

genetic disorder.

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b. Control group

This group included five healthy men, Sundanese, their ages ranged from 28 to 37 years

old.

Study Design

The current study was a cross-sectional study conducted in the Dermatology and

Venereology Clinic of Dr. Hasan Sadikin General Hospital, Bandung, Indonesia between

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May and July 2018. All the patients were subjected to careful history taking, physical

examination, local genital examination, laboratory investigations, and testicular

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ultrasonography examination. Semen analysis was performed in 10 patients who consented

(Figure 1).
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A record was made of each patient’s history of marital status, number of children, libido,
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erectile dysfunction, presence of erythema nodosum leprosum (ENL), duration of disease,

bacteriological index (BI) at diagnosis, and early treatment (≤ 1 year since onset of leprosy
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symptoms). Physical examination included, in particular testicular involvement, sexual hair

pattern and the presence of gynecomastia. Serum concentration of testosterone was measured
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using enzyme immunoassay technique (ELISA) (DiaMetra, Spello, Italia). Serum FSH and

LH levels were estimated using chemiluminescent immunoassay (CLIA) (Siemens Healthcare

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Diagnostics Inc, New York, USA). The results of FSH and LH were expressed as IU/L and
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testosterone as ng/ml. FSH, LH, and testosterone concentration of 1.4-18.1 IU/L, 1.5-9.3

IU/L, and 2.12-6.01 ng/ml, respectively were considered normal. Testicular volume was

measured using ultrasonography and volume of ≥ 15 ml were interpreted as normal, while

< 15 ml were considered reduced or atrophy. Seminal fluid was collected by masturbation

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after an abstinence period of at least three days. Sperm count, motility, and morphology were

determined according to the WHO recommendations.

Statistical analysis

Statistical analysis was conducted using statistical package for social sciences (SPSS)

version 24.0 for Windows. All collected data were then manually added to the patient’s

medical records, and the information was processed and analyzed using descriptive approach.

The data were presented as percentage (%) for categorical variables, and as mean ± standard

deviation (SD) and range for numerical variables.

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Ethics statements

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The study was approved by the ethical committee of Dr. Hasan Sadikin Hospital, affiliated
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with Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia (project number

LB.04.01/A05/EC/119/IV/2018). The patients were informed that they could withdraw from
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the study any time. Information of the patients were kept confidential. Written consent for
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participation in the study was obtained from each participant in their local language. For

children under the age of 18, consent was obtained from their parents or guardian.
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Results

Mean age of the patients was 29.87 ± 7.25 years (mean ± SD; range 16-40 years). Twenty-
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one (65.62%) patients were married and had children before the onset of leprosy. Of these, 32
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patients, 13 were borderline lepromatous (BL), 10 were lepromatous leprosy (LL), eight were

borderline borderline (BB), and one was borderline tuberculoid leprosy (BT). The duration of

disease in patients ranged from 4 months to 23 years with mean duration of 3.42 ± 4.04 years.

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Four (12.9%) patients had a BI ≥ 5. Twenty-six (81.25%) patients were still on treatment and

six (18.75%) had completed treatment. Fifteen (46.67%) patients received early treatment.

Five of the 32 (15.63%) patients had a history of ENL, two of those had a history of orchitis.

Reduced testicular volume was observed in 93.75% patients. The mean testicular volume

was 9.71 ± 3.98 ml each (mean ± SD). Based on the patients’ assessments, clinical

manifestations of testicular atrophy occurred in 10 (31.28%) patients. Some of these patients

had more than one clinical manifestation (Table 1). Libido was diminished in seven (21.87%),

female pubic hair pattern was observed in three (9.38%), gynecomastia in two (6.25%), and

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secondary infertility in two (6.25%) patients. None of the patients had erectile dysfunction

and primary infertility (Table 2).

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Serum testosterone was low in 13 (40.62%) patients with a mean of 2.64 ± 1.73 ng/ml.
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Serum LH and FSH were found to be elevated in 28.13% and 21.88% patients, respectively

(Table 3). The mean level of LH and FSH were 10.41 ± 12.69 IU/L and 16.47 ± 21.58 IU/L,
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respectively. Among the 32 patients, 16 (50%) had all the three hormones (testosterone, LH,
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and FSH) within the normal range; three (9.38%) had normal testosterone but elevated LH;

and six (18.75%) had low testosterone with elevated LH (Table 4).

Most of the patients refused to perform masturbation because of their religious beliefs.
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Semen analysis was therefore carried out in only 10 patients: four showed teratozoospermia,

two oligoteratozoospermia, two oligoasthenoteratozoospermia, one oligospermia, and one

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azoospermia. The mean sperm count was 15.98 ± 18.77 million/ml (mean ± SD) with normal
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reference value being ≥ 15 million/ml. However, the clinical manifestations, hormonal

profile, testicular volume, and semen analysis examination according to type of leprosy could

be seen on table 5. All individuals in the control group were normal.

Discussion

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 The testicles are among the most commonly involved organs in leprosy (Saporta and

Yuksel, 1994). Grabstald and Swan (Grabstald and Swan (1952)) first reported that leprosy

affects the testicles. The testicular volume is correlated significantly with testosterone level

(Hasan et al., 2017). Therefore, measurement of testicular volume using an ultrasonography

may be an important clinical tool to identify those at risk of testicular atrophy. In the current

study, we found that 93.75% of our patients had reduced testicular volume. This is a high

percentage compared to other studies which reported testicular involvement in 10-50% of

cases (Saporta and Yuksel, 1994). As the disease progresses, more of our patients presented

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with testicular atrophy.

Testosterone is the most important testicular androgen in men. Testosterone level

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decreases about 1% per year after the age of 40 while in leprosy patients, serum testosterone
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level decreases as a result of testicular atrophy; in contrast, serum LH level increases due to

decreased negative feedback from testosterone (Aglamis et al., 2014). High levels of serum
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LH indicated damage to the Leydig cells (Leal and Foss, 2009). This study observed that
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40,62% patients had low testosterone level. In addition, 9,38% patients had normal

testosterone level but elevated LH, which may indicate early testicular atrophy. This condition

is due to slight destruction of Leydig cells (Levis et al., 1989). These findings were consistent
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with that of other studies (Hasan et al., 2017; Levis et al., 1989).

The hormone inhibin is secreted primarily by Sertoli cells in the seminiferous tubules
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(Costabille 2013). The functions of this hormone include supressing FSH secretion and
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inhibiting mammotropic hormone. The absence of this hormone due to hyalinization of the

seminiferous tubules result an increase in the production of FSH and gynecomastia (Grabstald

and Swan, 1952). Gynecomastia has been reported in 25% and 27% LL patients in studies of

Elkawi et al. and Saporta, respectively (Elkawi et al., 2014; Saporta and Yuksel, 1994). In the

current study, 6,25% patients had gynecomastia.

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 The clinical manifestations of low testosterone include loss of libido, erectile dysfunction,

and changes in secondary sexual characteristics (female pubic hair pattern) (Andrade et al.,

2012). Saporta and Yuksel (Saporta and Yuksel (1994) reported diminished libido, erectile

dysfunction, and female pubic hair pattern in 29%, 56%, and 17% cases, respectively. Migam

et al. found 56,6% patients had sexual symptoms in the form of impotence and loss of libido

(Migam et al., 1984). The clinical manifestations vary throughout studies based on the factor

that affects testicular atrophy. Testicular involvement in leprosy might occur in the absence of

signs and symptoms (Leal and Foss, 2009). Measurement of testosterone levels repeatedly

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over the course of the disease may be needed to confirm the testicular atrophy (Hasan et al.,

2017). We did not observe a higher frequency of signs and symptoms in patients with low

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testosterone levels. These symptoms was presence in accordance to the degree of severity of
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low testosterone. However, the presence of signs and symptoms with abnormal hormone

levels, definitely indicate testicular atrophy (Hasan et al., 2017).

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There are few studies of fertility in patients with leprosy; one of these studies, conducted
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by Kumar et al. reported sterility in 28% of patients in India. Oligospermia and azoospermia

have been documented through semen analysis in 69% of lepromatous patients (Kumar et al.,

1982). Our study of semen analysis in 10 patients showed abnormality of sperm either in
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quality or quantity.

Histopathological changes of testicular involvement in leprosy were first described and

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classified by Grabstald and Swan, into three different phases: vascular (active leprous
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orchitis), interstitial, and obliterative; and by Job, into four stages: invasion, acute

inflammation, resolution, and atrophy (Grabstald and Swan, 1952). In the vascular phase, the

lymphocytes infiltrate the vessels of all sizes, resulting in the thickening of the vessel walls

and narrowing of the lumen. There are numerous lymphocytes and acid-fast bacilli (AFB)

residing perivascularly. During this phase, the seminiferous tubules, Sertoli cells, and

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interstitial cells of Leydig are unaffected (Grabstald and Swan, 1952; Migam et al., 1984).

The interstitial phase exhibits signs of progressive reactive obliterative endarteritis, but the

prominent changes typically consist of masses of Leydig cells clumps and interstitial fibrosis.

There are diffuse collagen deposition with aggregates of Leydig cells in the interstitial tissues

(Grabstald and Swan, 1952). The seminiferous tubules are seen to be relatively smaller.

Sometimes spermatogonia are seen, but no mature spermatozoa are found. (Grabstald and

Swan, 1952;Migam et al., 1984). In the final stage or obliterative phase, fibrosis is prominent,

resulting in obliteration and hyalinization of seminiferous tubules. This progressive fibrosis

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might cause reduced blood supply, leading to damages to the Leydig cells. This progressive

destruction explains the presence of low-grade spermatogenesis and atrophy of the testicles

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(Migam et al., 1984).
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In the current study, secondary infertility was observed in two patients. Infertility appeared

to be associated with disease progression. These results were consistent with that of Shilo et
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al. who reported that children were born to patients with leprosy during the first few years of
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the disease (Shilo et al., 1981). Saporta and Yuksel suggested that testicular damage may

occur before and while taking antileprotic treatment (Saporta and Yuksel, 1994).

Many factors may contribute to testicular atrophy, including the degree of testicular
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involvement, duration of disease, early administration of treatment, and the frequency or

intensity of orchitis resulting from ENL (Saporta and Yuksel, 1994; Elkawi et al., 2014).
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BI at diagnosis also one of the important factor to testicular atrophy (Hasan et al., 2017).
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These findings were similar with our study, involvement of testis occurs more often towards

lepromatous end of leprosy. There is an increase in interleukin (IL)-6, IL-8, and IL-10 levels

in ENL. It has been shown that LH and FSH were positively correlated with IL-1β, IL-6, and

tumor necrosis factor (TNF)-α while testosterone was inversely correlated with IL-6 and

TNF-α (Leal and Foss, 2009; Foss and Motta, 2012). This supports the theory that the

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inflammatory cytokine suggest to contribute in the local control mechanisms of testosterone

synthesis in the Leydig cells by blocking gonadotropin actions or inhibiting steroidogenesis

enzymatic activity (Foss and Motta, 2012). In 30 patients with testicular atrophy in the current

study, only two had an ENL attack with orchitis. Saporta and Yuksel analyzed that 51% of

their patients had reduced testicular size, and 71% of those had an ENL attack (Saporta and

Yuksel, 1994).

The strengths of the current study lie in the fact that we assessed testicular atrophy in

leprosy patients comprehensively through clinical manifestation, hormonal profile, testicular

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volume, and semen analysis. The study is limited by the small number of participants to

perform semen analysis; however, publications of testicular atrophy in leprosy patient are

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scarce and, therefore these data should prove to be very useful for future studies.
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In conclusion, the study showed a high frequency of testicular atrophy in Indonesian

leprosy patients with predominance silence symptoms. Therefore, the testicular function
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examination should recommend as a routine work-up for leprosy patients.
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Funding

This study was supported by a grant from Universitas Padjadjaran, Bandung, West Java,
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Indonesia (Grant no. 4851/UN6.C/LT/2018). The funders had no role in the study design, data

collection and analysis, decision to publish, or preparation of the manuscript.

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Ethics statements

The study was approved by the ethical committee of Dr. Hasan Sadikin Hospital, affiliated

with Faculty of Medicine, Universitas Padjadjaran, Bandung, Indonesia (project number

LB.04.01/A05/EC/119/IV/2018). The patients were informed that they could withdraw from

the study any time. Information of the patients were kept confidential. Written consent for

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participation in the study was obtained from each participant in their local language. For

children under the age of 18, consent was obtained from their parents or guardian.

Conflict of interests

The authors have declared that no competing interests exist.

Acknowledgment

The authors would like to extend their gratitude to the staff of the Department of Dermatology

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and Venereology, Faculty of Medicine, Universitas Padjadjaran who contributed to this work

and the patients for their participation in this study.

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References

Abd-Elkawi, Bahgat SA, Kamel AM, Farag AS, Ashor AM. Testicular function in male
patients with lepromatous leprosy. Egypt J Dermatol Venereol. 2014;34:41-5.
Achdiat, PA, Fadilla Y, Gunawan H, Suwarsa O. Testicular atrophy and its clinical
manifestatioins in a patient released from leprosy treatment. Lepr Rev. 2018;89:83-6.
Aglamis E, Tasdemir C, Yucel MO, Ceylan C, Erden I. Prostatic and testicular parameters in
lepromatous patients. Lepr Rev. 2014;85:48-53.
Andrade LJO, Oliveira MF, Franca LS, Souza ALOF, Andrade CS, Jesus HB.
Hypogonadism in leprosy males. R Ci Med Biol. 2012;11(1):60-3.
Costabille R. Anatomy and physiology of male reproductive system. 2013. [Accessed 25

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April 2019]
https://pdfs.semanticscholar.org/ee52/ce4c7f9335452e6b63eef70d2f532b555cb6.pdf.

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El- Beheiry A, Zeid SA, El- Ghazzawi E, Mansy E, Salama N. The leprous testis. Arch
Androl. 1979;3(2):173-6.
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Foss NT, Motta ACF. Leprosy, a neglected disease that causes a wide variety of clinical
conditions in tropical countries. Mem Inst Oswaldo Cruz. 2012;107(1):28-33.
Grabstald H, Swan LL. Genitourinary lesions in leprosy with special reference to the problem
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of atrophy of the testes. JAMA. 1952;149(14):1287-91.
Hasan M, Quyum F, Rahman MA, Panthi S. Testicular dysfunction in men affected by
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lepromatous leprosy. Lepr Rev. 2017;88:258-64.

Kumar B, Raina A, Kaur S, Dash RJ, Samuel E, Datta BN. Clinico-pathological study of
testicular involvement in leprosy. Leprosy India. 1982;54:48-55.
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Leal AMO, Foss NT. Endocrine dysfunction in leprosy. Eur J Clin Microbiol Infect Dis.
2009;28:1-7.
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Levis WR, Lanza AP, Swersie S, Meeker HC, Schuller GB, Bardin CW. Testicular
dysfunction in leprosy: relationships of FSH, LH, and testosterone to disease classification,
activity, and duration. Lepr Rev. 1989;60:94-101.
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Migam P, Mukhija RD, Gupta AK, Dayal SG, Goyal BM. Gonadal involvement in leprosy-
study of gynaecomastia, testicular and epididymal involvement and therapeutic efficacy of
indigenous drugs. Hansenol Int. 1984;9(1-2):10-20.
Saporta L, Yuksel A. Androgenic status in patients with lepromatous leprosy. Br J Urol Int.
1994;74:221-4.

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Shilo S, Livshin Y, Sheskin J, Spitz IM. Gonadal function in lepromatous leprosy. Lepr Rev.
1981;52:127-34.
Singh RK, Bhasin R, Kumar KVS. Endocrine dysfunction in patients of leprosy. Indian J
Endocrinol Metab. 2015;19(3):369-72.

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Table and figure legends

Figure 1. Study design

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Table 1. Clinical manifestations of testicular atrophy in each patient

Table 2. Symptoms of testicular atrophy

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Table 3. Hormonal profile of patients

Table 4. Testosterone and LH levels of patients

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Table 5. Testicular atrophy according to type of leprosy

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Table 1. Clinical manifestations of testicular atrophy in each patient

Clinical Manifestations No. patients, n=32 %

Testicular dysfunction 10 31.28

Loss of libido 4 12.50
Erectile dysfunction 0 0.00
Female pubic hair pattern 1 3.13
Gynecomastia 1 3.13
Infertility
Primary 0 0.00
Secondary 1 3.13
Loss of libido and female pubic hair pattern 1 3.13
Loss of libido and secondary infertility 1 3.13
Loss of libido and female pubic hair pattern and 1 3.13
gynecomastia
No testicular dysfunction 22 68.72

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Table 2. Symptoms of testicular atrophy

Symptoms No. patients, n=32 %

Loss of libido 7 21.87

Erectile dysfunction 0 0.00
Female pubic hair pattern 3 9.38
Gynecomastia 2 6.25
Infertility
Primary 0 0.00
Secondary 2 6.25

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Table 3. Hormonal profile of patients

Hormonal Profile No. patients, n=32 %

Serum testosterone
Normal 19 59.38
Decreased 13 40.62

Serum LH
Normal 23 71.87
Elevated 9 28.13

Serum FSH
Normal 25 78.12
Elevated 7 21.88

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*LH: Luteinizing hormone, FSH: Follicle stimulating hormone

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Table 4. Testosterone and LH levels of patients

LH Normal LH Elevated
No. patients % No. patients % No. patients %

Testosterone
Normal 16 50.00 3 9.38 19 59.38
Decreased 7 21.87 6 18.75 13 40.62

Total 23 71.87 9 28.13 32 100

*LH: Luteinizing hormone

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Table 5. Testicular atrophy according to type of leprosy

Testicular atrophy Lepromatous Borderline Borderline Borderline

Leprosy Lepromatous Borderline Tuberculoid
(n=10) (n=13) (n=8) (n=1)
Clinical manifestations
- Loss of libido 6 0 1 0
- Female pubic hair pattern 3 0 0 0
- Gynecomastia 2 0 0 0
- Secondary infertility 1 1 0 0
Hormonal profile:
- Elevated LH dan FSH level 4 1 1 0
- Low testosterone 7 3 2 1
Reduced testicular volume 10 11 8 1

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Semen analysis:
- Oligospermia 1 0 0 0
- Teratozoospermia 0 3 1 0
0 0 2 0

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- Oligoteratozoospermia
- Oligoasthenoteratozoospermia 0 1 1 0
- Azoospermia 1 0 0 0

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